The proposed study will define factors which regulate and enhance renal regeneration following acute toxic tubular injury and renal compensatory growth following contralateral uninephrectomy. Objectives of the investigation are to: A. Characterize altered renal membrane metabolism during the induction and healing of mercuric chloride induced acute tubular necrosis in the rat by measuring changes in phospholipid metabolism in kidney slices. Increased phospholipid synthesis may be an initiating event in renal regeneration after toxic injury since it occurs within 5 minutes after the onset of renal compensatory growth following uninephrectomy. B. Isolate and characterize humoral and tissue factors which mediate renal compensatory growth and renal regeneration with an in vitro bioassay which utilizes the rapid increase in renal phospholipid synthesis during compensatory growth as a detector of renal growth-promoting activity. C. Evaluate the efficacy of specific amino acids given in the diet to enhance recovery from acute tubular necrosis by measuring alterations in renal glomerular and tubular function. The biochemical correlates of renal cellular regeneration will be assessed in vitro by measuring phospholipid, protein, RNA and DNA synthesis and amino acid transport. D. Determine the capacity of various macromolecular precursors in vitro to enhance the biochemical indices of renal regeneration in kidney slices from animals recovering from acute tubular necrosis. The long term goals of the proposed study are to provide a biochemical basis for the rational treatment of acute injury of the kidney and of other organs as well. BIBLIOGRAPHIC REFERENCES: Ordonez, N.G., Toback, F.G., Aithal, H.N. and Spargo, B.H. Zonal changes in renal structure and phospholipid metabolism during reversal of potassium depletion nephropathy. Lab. Invest. 36:33-47, 1977. Toback, F.G., Havener, L.J., Dodd, R.C., and Spargo, B.H. Phospholipid metabolism during renal regeneration after acute tubular necrosis. Am. J. Physiol. Feb., 1977, in press.